Abstract
The thesis aims were to explore 1) genetic underpinnings of apathy in schizophrenia spectrum disorders (SZ) and healthy controls (HC), 2) prevalence of persistent apathy (PA), persistent depression (PD) and associations with functioning in a 1-year follow-up study of first-episode psychosis (FEP), 3) predictors and development of apathy, and associations with functioning in a 10-year follow-up study of FEP and HC.
In HC, apathy was stable and low during the 10-year follow-up. In FEP, apathy decreased the first year and then remained stable. The duration of untreated psychosis (DUP), baseline apathy and depression scores were positively associated with apathy development. The effects of DUP and baseline apathy were enduring, but the effect of depression abated. Almost 40% had PA and/or PD the first year. A significant overlap of PA and PD was found in 11%. Having PA, PD or both was associated with severely impaired functioning, compared to having no persistent symptoms. Apathy showed negative cross-sectional associations with functioning during the 10-year follow-up. In SZ and HC, apathy showed non-significant associations with a schizophrenia polygenic risk score (SZ PRS). SZ PRS did not contribute to the explained variance in apathy in SZ.
The consistent, negative associations with functioning affirm the enduring impact of apathy in FEP. The first year may be a critical period. Here, apathy is less cemented and maybe more responsive to treatment. Predictors of an unfavorable apathy course present early and may help clinicians identify a vulnerable subgroup in FEP. After one year, individuals with PA, PD, or both, have severe functional impairments. Thus, one should explore depressive symptoms in those with apathy and vice versa, use rating scales that reliably discriminate these similar phenotypes, and treat depression if present. Apathy may not be linked to the common genetic architecture of SZ. Research into environmental factors underlying apathy is warranted.